Anchorage-dependent cell cycle progression.
Anchorage-dependent cell cycle progression.
复制标题
DOI：
10.1083/jcb.136.1.1
复制
发表时间：
1997-01-13
期刊：
影响因子：
--
通讯作者：
Assoian RK
中科院分区：
文献类型：
--
作者：
Assoian RK
锚定依赖性生长的概念以及锚定独立性和致瘤性之间的密切关系在四分之一个多世纪前首次被认识到（9，16，23，24）。Penman和他的同事随后表明，在没有基质（例如，组织培养塑料或纯化的细胞外基质蛋白[ECM]）的情况下孵育细胞会抑制mRNA的产生和蛋白质的合成（2）。随着细胞转化程度的增加，这些影响变得不那么明显（27）。Folkman实验室表明，贴壁依赖性细胞的增殖需要一种铺展的细胞形状，而不是粘附本身（8）。像生长因子的作用一样，细胞锚定和细胞形状的生长调节作用映射到细胞周期的G1期。随着最近关于细胞周期控制的信息的爆炸，特别是细胞周期蛋白依赖性激酶（cdks），我们已经开始发展一个分子图像，现在可以解释哺乳动物细胞生物学的这些基本原则。
The concept of anchorage-dependent growth and the close relationship between anchorage independence and tumorigenicity were first appreciated more than a quarter century ago (9, 16, 23, 24). Penman and his coworkers then showed that incubation of cells in the absence of substratum (eg, tissue culture plastic or purified extracellular matrix protein [ECM]) resulted in an inhibition of mRNA production and protein synthesis (2). These effects became less pronounced with increasing degrees of cell transformation (27). The Folkman laboratory showed that a spread cell shape, rather than adhesion per se, was required for the proliferation of anchoragedependent cells (8). Like the effects of growth factors, the growth regulatory effects of cell anchorage and cell shape mapped to the G1 phase of the cell cycle. With the recent explosion of information about cell cycle control in general, and cyclin-dependent kinases (cdks) 1 in particular, we have begun to develop a molecular picture that can now explain these fundamental tenets of mammalian cell biology.